To successfully infect, Trypanosoma cruzi evades and modulates the host immune response. T. cruzi calreticulin (TcCalr) is a multifunctional, endoplasmic reticulum (ER)-resident chaperone that, translocated to the external microenvironment, mediates crucial host–parasite interactions. TcCalr binds and inactivates C1 and mannose-binding lectin (MBL)/ficolins, important pattern- recognition receptors (PRRs) of the complement system. Using an apoptotic mimicry strategy, the C1–TcCalr association facilitates the infection of target cells. T. cruzi infection also seems to confer protection against tumorigenesis. Thus, recombinant TcCalr has important antiangiogenic properties, detected in vitro, ex vivo, and in ovum, most likely contributing at least in part, to its antitumor properties. Consequently, TcCalr is useful for investigating key issues of host–parasite interactions and possible new immunological/pharmacological interventions in the areas of Chagas' disease and experimental cancer.

为了成功感染，克氏锥虫逃避并调节宿主的免疫反应。克鲁氏梭菌钙网蛋白（TcCalr）是一种多功能的内质网（ER）分子伴侣，可转移至外部微环境，介导重要的宿主-寄生虫相互作用。TcCalr结合并灭活补体系统的重要模式识别受体（PRR）C1和甘露糖结合凝集素（MBL）/纤维蛋白。使用凋亡模拟策略，C1-TcCalr关联可促进靶细胞的感染。克鲁维氏梭菌感染似乎也赋予了抗肿瘤发生的保护作用。因此，重组TcCalr具有重要的抗血管生成特性，可以在体外，离体和体外检测到。在卵子中，最有可能至少部分地有助于其抗肿瘤特性。因此，TcCalr可用于研究美洲锥虫病和实验性癌症领域中宿主与寄生虫相互作用的关键问题以及可能的新的免疫学/药理学干预措施。